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Spinal cord phosphoproteome of SCA2/ALS13 mouse model

ABSTRACT: Toxic polyglutamine (polyQ) expansions in ATXN2 trigger neurodegenerative processes, causing Spinocerebellar Ataxia type 2 (SCA2), and enhancing TDP 43-dependent pathology in Amyotrophic Lateral Sclerosis (ALS) / Fronto-Temporal Dementia (FTD). Primary disease events can be compensated transiently, delaying disease manifestation. To define potential therapy targets, we documented how cells modify their phospho-signals and how the ATXN2 interactome changes, using preferentially affected nervous tissues from end-stage Atxn2-CAG100-KnockIn mice.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Spinal Cord

SUBMITTER: Jana Key

LAB HEAD: Georg Auburger

PROVIDER: PXD062823 | Pride | 2025-09-29

REPOSITORIES: Pride

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			Action	DRS
	20210303_Swissprot_Mouse_ISO4prot.fasta	Fasta
	210308_32716_KA_L-017.raw	Raw
	210308_32717_KA_L-009.raw	Raw
	210308_32718_KA_L-008.raw	Raw
	210308_32719_KA_L-011.raw	Raw

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Publications

Spinal Cord Phosphoproteome of SCA2 Mouse Model Reveals Alteration of ATXN2-N-Term PRM-SH3-Actin Interactome and of Autophagy.

Almaguer-Mederos Luis-Enrique LE Kandi Arvind Reddy AR Sen Nesli-Ece NE Canet-Pons Júlia J Berger Luca-Malena LM Stokes Matthew P MP Abell Kathryn K Key Jana J Gispert Suzana S Auburger Georg G

Molecular & cellular proteomics : MCP 20250922 11

Toxic polyglutamine (polyQ) expansions in ataxin-2 (ATXN2) trigger neurodegenerative processes, causing spinocerebellar ataxia type 2, and enhancing TAR DNA-binding protein 43-dependent pathology in amyotrophic lateral sclerosis/frontotemporal dementia. Primary disease events can be compensated transiently, delaying disease manifestation. To define potential therapy targets, here we studied how cells modify phosphoprotein signals, using preferentially affected nervous tissue from end-stage Atxn2 ...[more]

PMID: 40992657

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